Journal
NEURON
Volume 46, Issue 2, Pages 191-204Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2005.01.030
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Funding
- NICHD NIH HHS [HD18655, K08 HD01384] Funding Source: Medline
- NIMH NIH HHS [R01 MH59894] Funding Source: Medline
- NINDS NIH HHS [NS45500, R01 NS045500, R01 NS35884] Funding Source: Medline
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Ephs regulate growth cone repulsion, a process controlled by the actin cytoskeleton. The guanine nucleotide exchange factor (GEF) ephexinl interacts with EphA4 and has been suggested to mediate the effect of EphA on the activity of Rho GTPases, key regulators of the cytoskeleton and axon guidance. Using cultured ephexin1(-/-) mouse neurons and RNA interference in the chick, we report that ephexinl is required for normal axon outgrowth and ephrin-dependent axon repulsion. Ephexin1 becomes tyrosine phosphorylated in response to EphA signaling in neurons, and this phosphorylation event is required for growth cone collapse. Tyrosine phosphorylation of ephexinl enhances ephexinl's GEF activity toward RhoA while not altering its activity toward Rac1 or Cdc42, thus changing the balance of GTPase activities. These findings reveal that ephexinl plays a role in axon guidance and is regulated by a switch mechanism that is specifically tailored to control Eph-mediated growth cone collapse.
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